title: The inhibitory influence of pulmonary vagal afferents on respiratory distress induced by airway occlusion in halothane-anesthetized cats.
abstract: Although the sensation of dyspnea is common, the mechanisms underlying the sensation have not been fully elucidated. Dyspnea, which is a subjective sensation induced by various respiratory and nonrespiratory stimuli, ranges in intensity from an awareness of difficulty in breathing to an incapacitating state of respiratory distress. It need not be an all or none concept when tolerable; however, intolerable dyspnea is often accompanied by some kind of escape response. In a previous study, we developed a new concept of minimum alveolar anesthetic concentration for airway occlusion (MAC-AOR). Using this model, we assessed the influence of pulmonary vagal afferents on respiratory distress induced by airway occlusion. Adult cats (n = 13) of both sexes weighing 2.7-5.6 kg (3.9 +/- 0.3 kg, mean +/- SE) were anesthetized with halothane and tracheally intubated. After determination of MAC-AOR, anesthesia was maintained with the highest concentration of halothane permitting the positive motor response identified by visual inspection or electromyogram (EMG) of the forearm, usually of the head or extremities. Twisting or jerking of the head was considered a positive response, but twitching or grimacing was not. A slight movement of the shoulder and/or the extremities was not considered positive, nor were coughing, swallowing and chewing, or rigidity recognized as the increase of tonic activity on the forearm EMG. The duration from the start of airway occlusion to the onset of the positive response (DOCCL) was considered as behavioral measures of the tolerable limit of respiratory distress. DOCCL was measured before (Control 1), during, and after (Control 2) lung expansion induced by the injection of the inhaled gas of 5 mL/kg or 10 mL/kg (LE5 or LE10) at functional residual capacity level. Subsequently, 6 of 13 cats received bilateral vagotomies, and the same procedure was repeated at the same concentration as stated above. Then, MAC-AOR after vagotomy was determined again. Before vagotomy, the values of DOCCL during lung expansion (238 +/- 30 s during LE5 and 288 +/- 24 s during LE10) were significantly longer than Control 1 (169 +/- 29 s) and Control 2 (154 +/- 29 s) values (P < 0.01). After vagotomy, the effect of lung expansion on DOCCL was totally abolished. MAC-AOR after vagotomy (1.4% +/- 0.1%) was significantly higher than that before vagotomy (1.1% +/- 0.1%) (P < 0.01). We have demonstrated that vagotomy abolishes the prolongation effect of the lung expansion on DOCCL and increases the value of MAC-AOR in this animal model. These results suggest that pulmonary vagal afferents play an important role in relief of respiratory distress developed during airway occlusion.
  
  
  CONCLUSIONS
  In anesthetized cats, we found that lung expansion reduces the tolerable limit to airway occlusion and vagotomy decreased minimum alveolar anesthetic concentration for airway occlusion, which suggests that pulmonary vagal afferents play an important role in relief of respiratory distress.
authors.affiliation: Department of Anesthesiology, Chiba University School of Medicine, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Sakurai
authors.forename: T
authors.initials: T
authors.lastname: Ide
authors.forename: M
authors.initials: M
authors.lastname: Aono
authors.forename: T
authors.initials: T
authors.lastname: Nishino
mesh_terms: D000344:Afferent Pathways; D000402:Airway Obstruction / Q000503:physiopathology*; D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D002415:Cats; D005260:Female; D006221:Halothane / Q000494:pharmacology*; D006339:Heart Rate; D006863:Hydrogen-Ion Concentration; D008168:Lung / Q000294:innervation*; D008297:Male; D010100:Oxygen / Q000097:blood; D012119:Respiration / Q000187:drug effects*; D014630:Vagus Nerve / Q000502:physiology*
chemical_list: D018685:Anesthetics, Inhalation; D002245:Carbon Dioxide; D010100:Oxygen; D006221:Halothane